Gout in Geese: Nutritional Factors Can Reduce Hyperuricemia by 60%! Mechanistic Study of NIC-1’s Action in Lowering Uric Acid (First Report)

Gout is a nutritional and metabolic disorder whose biochemical basis is hyperuricemia (HUA). Uric acid is only slightly soluble in the body’s blood environment; when its production far exceeds excretion, serum uric acid levels rise continuously. When these levels surpass solubility, sodium urate crystals form and deposit in tissues such as joints and kidneys, triggering inflammation. In severe cases, tophi develop, ultimately leading to gout. Poultry lack enzymes involved in urea synthesis, so ammonia produced from metabolizing ingested protein must be processed through purine nucleotide synthesis and degradation, with uric acid being the final excretory product. This process involves adenosine deaminase (ADA) and xanthine oxidase (XOD). Studies have shown that in goslings infected with goose astrovirus, the enzymatic activities and expression levels of ADA and XOD in the liver are significantly increased, enhancing uric acid synthesis and causing hyperuricemia and urate deposition, thereby inducing gout. The most appropriate strategies for reducing gout in geese involve nutritional interventions and vaccination. According to NIC’s comprehensive assessment, regulating nutrient concentrations while simultaneously adding active substances to modulate endogenous uric acid levels—thereby lowering creatinine and XOD activity—or incorporating active agents to inhibit goose astrovirus activity may prove to be an effective approach.

The R&D team at Guangdong Sanneng NIC has recently made groundbreaking progress in studying the pathogenesis of gout in goslings. Using a high-protein nutritional manipulation protocol, the team successfully established a gout model in goslings. The experiment was conducted at the Guangdong Sanneng NIC experimental base, where 192 Magang geese—half male and half female—were randomly assigned by body weight to four groups: a control group (CON), a high-protein modeling group (HP), an HP group receiving Qimei Su from day 1 (HP+QMS1), and an HP group receiving Qimei Su from day 14 (HP+QMS2). The modeling groups were fed diets containing 23.43% crude protein and 3.79% calcium. Each group had three replicates of 16 birds each, with a 14-day trial period. The goslings were housed in a brooding house maintained at 31°C initially, then kept at around 24°C. During the trial, birds had ad libitum access to water and feed under natural lighting; all other husbandry practices followed standard operating procedures. Body weights and feed intake were recorded for each group. The flock’s general condition, appetite, and fecal output were monitored. Any sick or dead birds were promptly assessed for clinical signs, necropsied, and examined for changes in internal organs such as the liver and kidneys, with post-mortem findings documented.

The kidneys are the only organs capable of secreting uric acid and play a primary role in its excretion; approximately 70% of the body’s uric acid is eliminated via the kidneys. Consequently, renal damage in poultry is a major cause of gout. Creatinine is a metabolic byproduct of muscle metabolism that is primarily cleared from the body by glomerular filtration without reabsorption; thus, serum creatinine levels reflect glomerular filtration function, and elevated serum creatinine indicates a decreased glomerular filtration rate. When the proximal tubules are damaged, excessive reabsorption or insufficient secretion of uric acid can lead to hyperuricemia.

During the trial, compared with the control group, geese in the HP modeling group exhibited lethargy, difficulty standing, frequent recumbency, markedly reduced appetite, and the passage of white, watery feces. Necropsy of dead geese revealed significant renal enlargement and visible whitening of the kidney surface. Taken together, these observations indicate that the clinical signs in the affected geese are consistent with the typical manifestations of visceral gout in geese.

Slaughter was performed on day 14 of the experiment, and sampling revealed the following findings:

Compared with the CON (control) group, goslings in the HP group had markedly enlarged, pale kidneys. Serum biochemical analyses showed that, compared with the control group, key biochemical indicators—uric acid, blood urea nitrogen, potassium, phosphorus, creatinine, and alkaline phosphatase—were significantly elevated in the serum of the gout model group. Excessively high serum uric acid, blood urea nitrogen, and creatinine levels indicate renal damage; in particular, excessive serum uric acid that precipitates on visceral surfaces is one of the main criteria for diagnosing visceral gout in goslings. Hepatic xanthine oxidase is a key enzyme in purine metabolism, and its activity is positively correlated with serum uric acid levels. Diets excessively high in protein and calcium promote conversion of xanthine dehydrogenase to xanthine oxidase. Xanthine oxidase catalyzes purine metabolism to produce more uric acid, nitric oxide, and reactive oxygen species, inducing inflammatory responses—redness, swelling, heat, and pain in joints or soft tissues—and worsening renal injury. Both clinical signs and biochemical indicators indicate that the high-protein, high-calcium diet in this experiment successfully established a gosling gout model. This conclusion is endorsed by Dr. Sun Minhua, Director of the Avian Diseases and Biotechnology Laboratory, Institute of Animal Health, Guangdong Academy of Agricultural Sciences.

The experimental results also showed that, in a high-protein gout model, supplementing the diet of Magang geese with 200 mg/kg of quimiase from one day of age to 14 days of age significantly reduced mortality and feed-to-gain ratio in the goslings while increasing feed intake. Biochemical analysis revealed that, Adding 200 mg/kg of bimatoprost significantly reduced serum levels of uric acid, xanthine oxidase, urea nitrogen, potassium, phosphorus, creatinine, and alkaline phosphatase in goslings, helping to alleviate gout symptoms and improve overall health. Notably, uric acid levels dropped from 500 to 190, a reduction of 60%! XOD is a key enzyme in purine metabolism; it not only increases uric acid (UA) production but also elevates intracellular reactive oxygen species (ROS) via pathways such as nitric oxide and calcium signaling. ROS can induce oxidative degradation, leading to the generation of numerous oxidases, which further increase oxygen free radicals and enhance oxidative reactions. Research on strategies to alleviate joint pain and suppress inflammatory responses for the prevention and treatment of gout attacks is of great significance. Therefore, a central component of gout management involves reducing XOD activity and enhancing the body’s antioxidant and anti-inflammatory capacities.

This study offers new insights into understanding and managing gout in goslings and holds promise for broad application in future farming practices. Furthermore, building on the successful development of a nutritional gout model, the NIC R&D team at Guangdong nuacid Company has continued its collaboration with the Institute of Animal Health of the Guangdong Academy of Agricultural Sciences to address viral gout in geese. This partnership positions the Guangdong nuacid NIC team to develop effective solutions targeting both nutritional and viral gout in geese.

Written by: E Xiaodi

Review: Hu Youjun